Statement on actinic keratosis: Actinic keratoses are cutaneous neopla
sms displaying chromosomal abnormalities that occur primarily on sun-e
xposed skin surfaces. These premalignant lesions are usually a consequ
ence of long-term solar radiation, but may also be caused by UV light
exposure from artificial sources, x-irradiation, or exposure to polycy
lic aromatic hydocarbons. Actinic keratoses range in size from 1 to 2
mm papules to large plaques. They may be flesh-colored, erythematous,
or more deeply pigmented, and they usually have a hyperkeratotic surfa
ce. Horn formation can occur in any location. Although it is usually p
ossible to diagnose actinic keratosis on the basis of the clinical app
earance of a lesion, it may on occasion be difficult (or impossible) t
o distinguish one from a squamous cell carcinoma of the skin and other
pathologic lesions without, doing a skin biopsy (or other procedure)
to obtain tissue for histologic examination. It has been demonstrated
that the p53 chromosomal mutation, found in more than 90% of human cut
aneous squamous cell carcinomas, is also present in actinic keratoses.
Estimates of the percentage of these chromosomally abnormal skin lesi
ons that convert to squamous cell carcinoma vary from 0.25% to 20% per
year for an individual lesion, Because patients often have multiple a
ctinic keratoses (because of the field effect of solar radiation), the
risks of conversion to a malignancy increase significantly. It is imp
ossible to predict accurately in which patient a squamous cell carcino
ma will develop. Most actinic keratoses and squamous cell carcinomas a
re asymptomatic. Once an actinic keratosis converts to a squamous cell
carcinoma, it may bleed, ulcerate, become infected, destroy anatomic
structures, or even spread to internal organs. Actinic keratoses must
be treated to prevent their conversion to squamous cell carcinoma. Tre
atment of these premalignant lesions avoids the potentially more invas
ive and extensive treatment of subsequent malignancy.